WNK4 Regulates Apical and Basolateral Cl-Flux in Extrarenal Epithelia
Mutations in the serine-threonine kinase WNK4 [with no lysine (K) 4] cause pseudohypoaldosteronism type II, a Mendelian disease featuring hypertension with hyperkalemia. In the kidney, WNK4 regulates the balance between NaCl reabsorption and K+secretion via variable inhibition of the thiazide-sensis...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2004-02, Vol.101 (7), p.2064-2069 |
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| creator | Kahle, Kristopher T. Gimenez, Ignacio Hassan, Hatim Wilson, Frederick H. Wong, Robert D. Forbush, Biff Aronson, Peter S. Lifton, Richard P. |
| description | Mutations in the serine-threonine kinase WNK4 [with no lysine (K) 4] cause pseudohypoaldosteronism type II, a Mendelian disease featuring hypertension with hyperkalemia. In the kidney, WNK4 regulates the balance between NaCl reabsorption and K+secretion via variable inhibition of the thiazide-sensistive NaCl cotransporter and the K+channel ROMK. We now demonstrate expression of WNK4 mRNA and protein outside the kidney. In extrarenal tissues, WNK4 is found almost exclusively in polarized epithelia, variably associating with tight junctions, lateral membranes, and cytoplasm. Epithelia expressing WNK4 include sweat ducts, colonic crypts, pancreatic ducts, bile ducts, and epididymis. WNK4 is also expressed in the specialized endothelium of the blood-brain barrier. These epithelia and endothelium all play important roles in Cl-transport. Because WNK4 is known to regulate renal Cl-handling, we tested WNK4's effect on the activity of mediators of epithelial Cl-flux whose extrarenal expression overlaps with WNK4. WNK4 proved to be a potent inhibitor of the activity of both the Na+- K+-2 Cl-cotransporter (NKCC1) and the Cl-/base exchanger SLC26A6 (CFEX) (>95% inhibition of NKCC1-mediated86Rb influx, P < 0.001; >80% inhibition of CFEX-mediated [14C] formate uptake, P < 0.001), mediators of Cl-flux across basolateral and apical membranes, respectively. In contrast, WNK4 showed no inhibition of pendrin, a related Cl-/base exchanger. These findings indicate a general role for WNK4 in the regulation of electrolyte flux in diverse epithelia. Moreover, they reveal that WNK4 regulates the activities of a diverse group of structurally unrelated ion channels, cotransporters, and exchangers. |
| doi_str_mv | 10.1073/pnas.0308434100 |
| format | Article |
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In the kidney, WNK4 regulates the balance between NaCl reabsorption and K+secretion via variable inhibition of the thiazide-sensistive NaCl cotransporter and the K+channel ROMK. We now demonstrate expression of WNK4 mRNA and protein outside the kidney. In extrarenal tissues, WNK4 is found almost exclusively in polarized epithelia, variably associating with tight junctions, lateral membranes, and cytoplasm. Epithelia expressing WNK4 include sweat ducts, colonic crypts, pancreatic ducts, bile ducts, and epididymis. WNK4 is also expressed in the specialized endothelium of the blood-brain barrier. These epithelia and endothelium all play important roles in Cl-transport. Because WNK4 is known to regulate renal Cl-handling, we tested WNK4's effect on the activity of mediators of epithelial Cl-flux whose extrarenal expression overlaps with WNK4. WNK4 proved to be a potent inhibitor of the activity of both the Na+- K+-2 Cl-cotransporter (NKCC1) and the Cl-/base exchanger SLC26A6 (CFEX) (>95% inhibition of NKCC1-mediated86Rb influx, P < 0.001; >80% inhibition of CFEX-mediated [14C] formate uptake, P < 0.001), mediators of Cl-flux across basolateral and apical membranes, respectively. In contrast, WNK4 showed no inhibition of pendrin, a related Cl-/base exchanger. These findings indicate a general role for WNK4 in the regulation of electrolyte flux in diverse epithelia. Moreover, they reveal that WNK4 regulates the activities of a diverse group of structurally unrelated ion channels, cotransporters, and exchangers.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0308434100</identifier><identifier>PMID: 14769928</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Antibodies ; Biological Sciences ; Blotting, Western ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Cell Polarity ; Chlorides - metabolism ; Complementary RNA ; Disease ; Enzymes ; Epithelium - metabolism ; Formates ; Gene expression regulation ; Humans ; Hypertension ; Immunohistochemistry ; Ion Transport ; Kidney - metabolism ; Kidneys ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Membrane Transport Proteins ; Mice ; Mutation ; Oocytes ; Oocytes - metabolism ; Physiological regulation ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; Radiocarbon ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Secretion ; Sodium-Potassium-Chloride Symporters - genetics ; Sodium-Potassium-Chloride Symporters - metabolism ; Solute Carrier Family 12, Member 2 ; Sweat ; Xenopus laevis</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2004-02, Vol.101 (7), p.2064-2069</ispartof><rights>Copyright 1993/2004 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Feb 17, 2004</rights><rights>Copyright © 2004, The National Academy of Sciences 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-ff6c32d84319ae489653ec42e8f9aa25bd6a63d05ff35bec5fd9bcd08bd1f2103</citedby><cites>FETCH-LOGICAL-c557t-ff6c32d84319ae489653ec42e8f9aa25bd6a63d05ff35bec5fd9bcd08bd1f2103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/101/7.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3371395$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3371395$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27903,27904,53770,53772,57996,58229</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14769928$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kahle, Kristopher T.</creatorcontrib><creatorcontrib>Gimenez, Ignacio</creatorcontrib><creatorcontrib>Hassan, Hatim</creatorcontrib><creatorcontrib>Wilson, Frederick H.</creatorcontrib><creatorcontrib>Wong, Robert D.</creatorcontrib><creatorcontrib>Forbush, Biff</creatorcontrib><creatorcontrib>Aronson, Peter S.</creatorcontrib><creatorcontrib>Lifton, Richard P.</creatorcontrib><title>WNK4 Regulates Apical and Basolateral Cl-Flux in Extrarenal Epithelia</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Mutations in the serine-threonine kinase WNK4 [with no lysine (K) 4] cause pseudohypoaldosteronism type II, a Mendelian disease featuring hypertension with hyperkalemia. In the kidney, WNK4 regulates the balance between NaCl reabsorption and K+secretion via variable inhibition of the thiazide-sensistive NaCl cotransporter and the K+channel ROMK. We now demonstrate expression of WNK4 mRNA and protein outside the kidney. In extrarenal tissues, WNK4 is found almost exclusively in polarized epithelia, variably associating with tight junctions, lateral membranes, and cytoplasm. Epithelia expressing WNK4 include sweat ducts, colonic crypts, pancreatic ducts, bile ducts, and epididymis. WNK4 is also expressed in the specialized endothelium of the blood-brain barrier. These epithelia and endothelium all play important roles in Cl-transport. Because WNK4 is known to regulate renal Cl-handling, we tested WNK4's effect on the activity of mediators of epithelial Cl-flux whose extrarenal expression overlaps with WNK4. WNK4 proved to be a potent inhibitor of the activity of both the Na+- K+-2 Cl-cotransporter (NKCC1) and the Cl-/base exchanger SLC26A6 (CFEX) (>95% inhibition of NKCC1-mediated86Rb influx, P < 0.001; >80% inhibition of CFEX-mediated [14C] formate uptake, P < 0.001), mediators of Cl-flux across basolateral and apical membranes, respectively. In contrast, WNK4 showed no inhibition of pendrin, a related Cl-/base exchanger. These findings indicate a general role for WNK4 in the regulation of electrolyte flux in diverse epithelia. Moreover, they reveal that WNK4 regulates the activities of a diverse group of structurally unrelated ion channels, cotransporters, and exchangers.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Biological Sciences</subject><subject>Blotting, Western</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Polarity</subject><subject>Chlorides - metabolism</subject><subject>Complementary RNA</subject><subject>Disease</subject><subject>Enzymes</subject><subject>Epithelium - metabolism</subject><subject>Formates</subject><subject>Gene expression regulation</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Immunohistochemistry</subject><subject>Ion Transport</subject><subject>Kidney - metabolism</subject><subject>Kidneys</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Membrane Transport Proteins</subject><subject>Mice</subject><subject>Mutation</subject><subject>Oocytes</subject><subject>Oocytes - metabolism</subject><subject>Physiological regulation</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Radiocarbon</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Secretion</subject><subject>Sodium-Potassium-Chloride Symporters - genetics</subject><subject>Sodium-Potassium-Chloride Symporters - metabolism</subject><subject>Solute Carrier Family 12, Member 2</subject><subject>Sweat</subject><subject>Xenopus laevis</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1v1DAQxS0EotvCmQtCUQ9wSjv-iu0Dh3a1BdQKJATiaDmO3WblTYKdoO1_j6NddQuHnkYz_r2ZZz2E3mA4wyDo-dCZdAYUJKMMAzxDCwwKlxVT8BwtAIgoJSPsCB2ntAYAxSW8REeYiUopIhdo9evrNSu-u9spmNGl4mJorQmF6Zri0qR-HsbcL0N5FaZt0XbFajtGE12Xp6uhHe9caM0r9MKbkNzrfT1BP69WP5afy5tvn74sL25Ky7kYS-8rS0mTzWJlHJOq4tRZRpz0yhjC66YyFW2Ae0957Sz3japtA7JusCcY6An6uNs7TPXGNdZ12UvQQ2w3Jt7r3rT635euvdO3_R9NuQBOsv79Xh_735NLo960yboQTOf6KWkJWBCJRQZP_wPX_RTzn5MmgClgxliGzneQjX1K0fkHIxj0HI-e49GHeLLi3WP_B36fxyNgVh7WYS3y4Wq--eFJQPsphNFtx0y-3ZHrNPbxAaVUYKo4_Qv8P6zL</recordid><startdate>20040217</startdate><enddate>20040217</enddate><creator>Kahle, Kristopher T.</creator><creator>Gimenez, Ignacio</creator><creator>Hassan, Hatim</creator><creator>Wilson, Frederick H.</creator><creator>Wong, Robert D.</creator><creator>Forbush, Biff</creator><creator>Aronson, Peter S.</creator><creator>Lifton, Richard P.</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040217</creationdate><title>WNK4 Regulates Apical and Basolateral Cl-Flux in Extrarenal Epithelia</title><author>Kahle, Kristopher T. ; 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In the kidney, WNK4 regulates the balance between NaCl reabsorption and K+secretion via variable inhibition of the thiazide-sensistive NaCl cotransporter and the K+channel ROMK. We now demonstrate expression of WNK4 mRNA and protein outside the kidney. In extrarenal tissues, WNK4 is found almost exclusively in polarized epithelia, variably associating with tight junctions, lateral membranes, and cytoplasm. Epithelia expressing WNK4 include sweat ducts, colonic crypts, pancreatic ducts, bile ducts, and epididymis. WNK4 is also expressed in the specialized endothelium of the blood-brain barrier. These epithelia and endothelium all play important roles in Cl-transport. Because WNK4 is known to regulate renal Cl-handling, we tested WNK4's effect on the activity of mediators of epithelial Cl-flux whose extrarenal expression overlaps with WNK4. WNK4 proved to be a potent inhibitor of the activity of both the Na+- K+-2 Cl-cotransporter (NKCC1) and the Cl-/base exchanger SLC26A6 (CFEX) (>95% inhibition of NKCC1-mediated86Rb influx, P < 0.001; >80% inhibition of CFEX-mediated [14C] formate uptake, P < 0.001), mediators of Cl-flux across basolateral and apical membranes, respectively. In contrast, WNK4 showed no inhibition of pendrin, a related Cl-/base exchanger. These findings indicate a general role for WNK4 in the regulation of electrolyte flux in diverse epithelia. Moreover, they reveal that WNK4 regulates the activities of a diverse group of structurally unrelated ion channels, cotransporters, and exchangers.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>14769928</pmid><doi>10.1073/pnas.0308434100</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Biological Sciences Blotting, Western Carrier Proteins - genetics Carrier Proteins - metabolism Cell Polarity Chlorides - metabolism Complementary RNA Disease Enzymes Epithelium - metabolism Formates Gene expression regulation Humans Hypertension Immunohistochemistry Ion Transport Kidney - metabolism Kidneys Membrane Proteins - genetics Membrane Proteins - metabolism Membrane Transport Proteins Mice Mutation Oocytes Oocytes - metabolism Physiological regulation Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Radiocarbon RNA, Messenger - genetics RNA, Messenger - metabolism Secretion Sodium-Potassium-Chloride Symporters - genetics Sodium-Potassium-Chloride Symporters - metabolism Solute Carrier Family 12, Member 2 Sweat Xenopus laevis |
| title | WNK4 Regulates Apical and Basolateral Cl-Flux in Extrarenal Epithelia |
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